Key result
Cardiotoxic antineoplastic therapy induced significant temporal increases in cardiac biomarkers, with median hs-cTnT rising from 5 ng/L at baseline to 15 ng/L at therapy completion.
Why the study?
Cardiotoxicity from antineoplastic therapies is an important clinical challenge, and early identification of subclinical cardiac injury may improve surveillance and long-term outcomes in cancer patients.
Cohort (n=90)
No
Absolute Event Rate: 15% vs 5%
p-value: p=<0.001
Serial assessment of hs-cTnT, NT-proBNP, and sST2 reveals distinct temporal trajectories of subclinical cardiac injury during cardiotoxic cancer therapy, which may aid in early cardiovascular surveillance.
Therapy-linked hs-cTnT rises support serial monitoring; leaves open prognostic value and intervention thresholds in cardio-oncology.
Background Cardiotoxicity associated with antineoplastic therapies remains an important clinical challenge in modern oncology. Early identification of subclinical cardiac injury may improve cardiovascular surveillance and long-term outcomes in cancer patients. Methods This prospective observational cohort study included 90 adult patients with breast cancer, lymphoma, or lung cancer receiving potentially cardiotoxic therapy. Patients with clinically manifest heart failure, severe arrhythmias, advanced renal disease, recent acute myocardial infarction, untreated severe valvular disease, or other major cardiovascular comorbidities were excluded. High-sensitivity cardiac troponin T (hs-cTnT), NT-proBNP, and soluble ST2 (sST2) were measured at baseline, during treatment, at therapy completion, and at late follow-up. Non-parametric tests were used for repeated-measures and subgroup comparisons. Results Significant temporal variations were observed for all biomarkers. hs-cTnT increased from 5 [3–8] ng/L at baseline to 15 [10–25] ng/L at T2, while NT-proBNP increased from 120 [80–190] pg/mL to 210 [150–320] pg/mL. sST2 demonstrated a delayed elevation and remained increased at follow-up. Distinct biomarker patterns were observed across malignancy subgroups, with higher hs-cTnT increases in breast cancer, more prominent NT-proBNP elevation in lymphoma, and higher sST2 values in lung cancer. Conclusions Serial biomarker assessment may provide complementary information on myocardial injury, ventricular stress, and fibrotic remodeling during cancer therapy. The observed biomarker trajectories are suggestive of different biological processes involved in therapy-related cardiotoxicity, but they should be interpreted in conjunction with imaging findings and clinical outcomes.
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Kajanto et al. (2026) conducted a cohort in Cancer receiving potentially cardiotoxic therapy (n=90). Potentially cardiotoxic antineoplastic therapy vs. Baseline (pre-treatment) was evaluated on Temporal variation of high-sensitivity cardiac troponin T (hs-cTnT) from baseline to therapy completion (p=<0.001). Cardiotoxic antineoplastic therapy induced significant temporal increases in cardiac biomarkers, with median hs-cTnT rising from 5 ng/L at baseline to 15 ng/L at therapy completion.
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